THE HEART
| CHEST PAIN —David Slattery, MD, Research Director, University Medical Center of Southern Nevada, Las Vegas
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| Introduction: know limitations of emergency department (ED) evaluation of chest pain (difficult to rule out disease in
short time); cannot rule out or exclude diagnosis of coronary artery disease (CAD) using history and physical examination,
single normal or unchanged electrocardiography (ECG), or single set of cardiac biomarkers; need to aggressively
treat patients with ST-elevation myocardial infarction (STEMI) and non-STEMI acute coronary syndrome (ACS; non-
STEMI ACS associated with higher mortality than STEMI); frequency of claims—ACS represents ≈10% of total claims
in ED, but almost one third of cost of claims paid out in emergency medicine results from missed diagnosis of ACS; costs
high because patients frequently in prime of life and because of association with significant mortality and long-term morbidity
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| Why claims occur: failure to diagnose (diagnosis not considered or diagnosis considered but inadequately or inappropriately
excluded); failure to provide treatment in timely manner; complications of treatment; failure to diagnose ACS
or non-STEMI causes of chest pain—occurs most often in young patients, patients with normal ECG or who present
with atypical chest pain, and in elderly patients presenting with shortness of breath; diagnosis considered, but inappropriately
excluded—majority of patients missed; can occur in young person with normal ECG and normal biomarkers;
failure to provide timely and aggressive treatment—American College of Cardiology/American Heart Association
(ACC/AHA) guidelines focus on 30 min door-to-drug time and 90 min door-to-balloon time or door-to-percutaneous coronary
intervention (PCI) time; new guidelines start clock ticking at time of first medical contact, ie, arrival of emergency
medical services (EMS), rather than arrival in ED; National Registry of Myocardial Infarction (NRMI) database provides
performance measures for care of patients with MI; majority of problems occur in patients with non-STEMI ACS; only
20% of hospitals in United States can provide full PCI capability; fibrinolytic therapy—preferred in patients presenting
within 3 hr; give if unable to get patient to catheterization laboratory within 90 min or if invasive strategy not option;
need protocol as backup to catheterization; work with EMS personnel so they know which patients should be at PCI facility,
ie, patients with high-risk STEMI, including those with congestive heart failure or cardiogenic shock, those in whom
fibrinolysis contraindicated, those who present after 3 hr, and those in whom diagnosis in doubt
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| Patient evaluation: document description of chest pain and use to stratify risk; include quality, duration, location and radiation,
migration, associated neurologic symptoms, possible aortic dissection, severity of onset, and whether pain exertion-
or stress-related; look for associated symptoms, eg, diaphoresis, nausea, dyspnea (usually indicates high risk);
document history of chest pain, CAD, and type of work-up; check for cardiac risk factors (ie, Framingham risk factors;
can use to stratify risk, but not predictive for individual patient); risk scoring—Thrombolysis in Myocardial Infarction
(TIMI) risk score predictive of risk for death, reinfarction, and target vessel revascularization; high-risk features include
ST-segment deviation (persistent or transient), T-wave inversion, and positive cardiac biomarkers; physical
examination—document vital signs, presence of diaphoresis, signs of acute heart failure, signs of peripheral vascular
disease, murmur/ectopy/rub (consider pericarditis), chest wall tenderness, and assessment of pulses (for aortic dissection)
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 | Diagnostic testing: obtain ECG within 10 min of arrival in ED; use ECG to classify patient as STEMI or new left bundle
branch block (LBBB); STEMI protocol involves PCI or fibrinolytic therapy; patients with ST depression or T-wave inversion
at high risk (high mortality rate); patients with normal or nondiagnostic ECG at low risk (not “no risk”; cannot
rule out disease); look for previous ECG; obtain chest x-ray to look for other causes of chest pain; look at cardiac (necrosis)
biomarkers, ie, creatine phosphokinase (CPK), CPK myocardial band (CPK-MB), cardiac troponin I and T, and
myoglobin, to determine damage to myocardium; can use ischemia markers, eg, ischemia-modified albumin (IMA);
obtain echocardiography to look for wall motion abnormalities; observation—provide cardiac monitoring, O2 , and
aspirin (unless contraindicated); treat pain; consider nitroglycerin to relieve symptoms; obtain serial vital signs, examinations,
and ECGs; repeat biomarkers; provocative testing—perform once necrosis ruled out; consider exercise
treadmill test, technetium (Tc99m) sestamibi (Cardiolite) stress test, or cardiac catheterization
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| Limitations and value of ED data: presenting without chest pain—study found absence of chest pain in 33% of
patients with MI; patients with MI who most often present without chest pain include elderly, female patients, nonwhite
patients, and patients with history of diabetes, past congestive heart failure (CHF), or stroke; Global Registry of Acute
Coronary Events (GRACE) trial—looked at 20 881 patients with MI or ACS; found 8% of patients with diagnosed
STEMI and 12.3% of patients with diagnosed non-STEMI ACS presented without chest pain; presenting symptoms included
shortness of breath 49%, diaphoresis 26%, nausea and vomiting 24%, and syncope or near-syncope 19%; overall
hospital fatality rate of patients presenting without chest pain 13%, compared to 4.3% in patients who presented with
chest pain; Pope et al (2000)—study looked at missed diagnosis of acute cardiac ischemia in ED and found ≈8% of patients
had MI, and of these, ≈2% discharged home from ED; 2% of patients with unstable angina also discharged home;
risk factors for discharge include female sex, age <55 yr, nonwhite ethnicity, normal ECG, chief complaint of shortness
of breath; McCarthy et al (1993)—landmark study looking at missed diagnosis of acute MI in ED found 2% of patients
with acute MI not admitted to hospital; unadmitted patients less likely to have ischemic ECG changes and history of
CAD; 35% of patients had recognized ischemia on ECG review, and 25% had ST elevation; misdiagnoses included gastrointestinal
(GI) pain 20%, atypical chest pain 20%, musculoskeletal chest pain 10%; GI cocktail—used in patients
whose pain thought to be GI in origin; do not use to make or exclude diagnosis; Wren et al study looked at 97 patients
presenting with chest pain and given GI cocktail; positive response noted in 8 of 11 patients with myocardial ischemia;
nitroglycerin—study found response to nitroglycerin not reliable method to predict presence of cardiac etiology;
viscerotome—areas of esophagus, stomach, gallbladder, and heart that share common segmental innervation, making
cardiac pain difficult to distinguish from GI pain; chest wall tenderness and costochondritis—study found final diagnosis
of acute MI made in 6% of patients with costochondritis; accuracy of ECG—study found ED physicians had diagnostic
sensitivity of 81% and specificity of 69%; ability to rule out disease and diagnose ACS using ECG slightly better
than 50%; clinical utility of single cardiac biomarker—study looked at single ED test and found sensitivity of 40%
and specificity 80%; sensitivity 90% if 3-hr level added; do not discharge patient after getting single set of biomarkers,
even in patients with continuous chest pain over last 48 hr
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| Recommendations: varied presentations common, so keep index of suspicion high; semantics—patients do not want
to tell physician they have chest pain, so they complain of “discomfort” or “tightness”; screen patients and use ECG liberally;
beware of “variant angina”; shortness of breath most common presentation of acute MI in elderly patients; look
for complaints of shoulder and arm pain, neck and jaw pain, and epigastric pain; write “chest pain,” not “atypical chest
pain,” in discharge diagnosis; ECG—cornerstone of risk stratification scheme; remember ACS dynamic process; obtain
ECG early and often; ECG reliable only if positive; negative ECG does not rule out disease; comparison with previous
ECG helpful, but unchanged ECG cannot be used to rule out disease; consider nonspecific ECG positive until proven otherwise;
cardiac biomarkers—reliable only if positive; single set of negative biomarkers cannot be relied on to rule out
necrosis; increased sensitivity and specificity associated with second set of enzymes; systems approach—get registry
data specific to institution (eg, NRMI) or do performance improvement (PI) measurement of STEMI and ACS care; risk
stratify patients; treat patients with high-risk features aggressively; develop systems for ruling out both phases of ACS
(ruling out necrosis; provocative testing); chest pain center can help exclude patients and identify patients for further testing;
develop clinical pathways and protocols; have reliable and consistent cardiology consultation available for patients
under observation; fibrinolytic therapy—avoid delay; standard protocol allows 30 min, beginning with EMS contact;
have preestablished protocols in ED; emergency physician should initiate fibrinolytic therapy when needed; discharge
instructions—should provide early follow-up and contain detailed instructions; understand limitations of work-up;
avoid precautionary antianginal treatment; do not send patient home on nitroglycerin; make sure patient has definite referral
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| UNRECOGNIZED KILLERS ON ECG —Amal Mattu, MD, Associate Professor, Department of Emergency Medicine,
and Program Director, Emergency Medicine Residency, University of Maryland School of Medicine, Baltimore
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| Brugada syndrome: first described ≈14 yr ago by Brugada brothers in southeast Asia in adolescent males who died in
sleep; hearts structurally normal at autopsy; completely electrical phenomenon; family history of abnormality in ≈50% of
cases; more common cause of sudden death than previously recognized; responsible for 4% to 5% of all sudden deaths
and up to 20% of cardiac arrests in individuals with structurally normal hearts; 1 in 25 nontraumatic cardiac arrests probably
statistically related to Brugada syndrome; most commonly seen in young men, but also can occur in young women;
first onset of symptoms occurs (on average) at ≈40 yr of age; mortality rate 10% per year if not recognized and treated;
0% mortality if recognized and treated with automatic implantable cardioverter defibrillator (AICD; only means of improving
mortality rate); after recognizing syndrome, send patient to electrophysiologist for definitive testing; ECG
findings—propensity for polymorphic or monomorphic ventricular tachycardia; abnormal ECG findings primarily in V1
and V2, but can also occur in V3 ; look for right bundle branch block (RBBB) or incomplete RBBB pattern with ST-segment
elevation; 2 types of ST elevation, “coved-type” (convex; most common) or “saddle-type” (concave; less common);
ECG findings vary, depending on many factors, eg, medications, body temperature, ambient temperature; patients do not
have pain; no reciprocal findings; patients usually asymptomatic when seen by ED physician
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| Hypertrophic cardiomyopathy: characterized by hypertrophied but nondilated left ventricle; cardiomegaly usually
not seen on chest x-ray; abnormality seen only on echocardiography (hypertrophy localized to septum, not entire ventricle);
patients have normal heart size until late-stage disease when left ventricle dilated; family history in ≈50% of patients;
average age at diagnosis 30 to 40 yr; mortality rate 3.5% per year; pathophysiology unknown; clinical features include syncope,
chest pain, palpitations, and dyspnea sometimes associated with exertion; usually sudden death related to dysrhythmia
or sudden reduction in cardiac output; classically, patients have systolic murmur that changes with position or physical
maneuvers, but not all patients have easily audible murmur; definitive diagnosis made with Doppler echocardiography to
identify left ventricular outflow obstruction; treat initially with β-blockers or calcium channel blockers; start patient with
ventricular dysrhythmia on amiodarone; ECG findings—patients have high left ventricular voltage (HLVV); very tall
QRS complexes throughout most of ECG; up to 50% of patients have deep narrow Q waves in lateral leads I, aVL, V5 , and
V6 ; patients often misdiagnosed as having lateral MI, but infarction Q waves not present
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| Prolonged QT interval: keep index of suspicion high in patients with syncope or near-syncope; probably more common
cause of syncope and sudden death than previously recognized; differential diagnosis—electrolyte abnormalities
(eg, hypokalemia, hypocalcemia, hypomagnesemia; easily reversible); sodium channel-blocking medications (eg, type 1A
antiarrhythmic agents, anticholinergics, cocaine, many antipsychotics, some antibiotics; also reversible cause); severe intracranial
bleeding; cerebral edema from hyponatremia, eg, due to overdose of 3,4-methylenedioxymethamphetamine
(MDMA; Ecstasy); acute cardiac ischemia, hypothermia, and hereditary causes; prolongation—how long is too long? literature
suggests patient at high risk for development of arrhythmia, especially torsades de pointes, if QTc ≥ 500 msec; torsades
de pointes—polymorphic ventricular tachycardia associated with prolonged QT interval; multiple modes of
treatment for polymorphic ventricular tachycardia; however, in patients with torsades de pointes, amiodarone, procainamide,
and lidocaine contraindicated because of prolonged QT interval; management—find and treat underlying cause,
eg, correct electrolyte abnormality or discontinue responsible medications; in patients with congenital or idiopathic
causes, use β-blocker; to treat torsades de pointes, cardioversion/defibrillation, magnesium if patient stable, or magnesium
after cardioversion; overdrive pacing and isoproterenol rarely necessary; clinical pearl—in patients who present
with gastroenteritis severe enough to warrant measurement of electrolytes, obtain initial ECG to look for prolonged QT
interval
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Educational Objectives
| The goal of this activity is to provide a greater understanding of the management of chest pain and unrecognized
causes of sudden death in emergency electrocardiography. After hearing and assimilating this program, the clinician
will be better able to:
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| 1. Evaluate a patient with chest pain in the emergency department (ED).
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| 2. Discuss the limitations and value of the evaluation and treatment of chest pain in the ED.
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| 3. Describe how to improve the management of patients with chest pain in the ED.
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| 4. Describe the features of Brugada syndrome.
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| 5. Evaluate a patient for hypertrophic cardiomyopathy and prolonged QT interval.
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Discussed on This Program
Amiodarone HCl [Cordarone, Pacerone]
Aspirin (acetylsalicylic acid; ASA)[several trade names]
Lidocaine HCl [several trade names]
Nitroglycerin [several trade names]
Procainamide HCl [Procanbid]
Suggested Reading
Antzelevitch C: Brugada syndrome. Pacing Clin Electrophysiol 29:1130, 2006; Boie ET: Initial evaluation of
chest pain. Emerg Med Clin North Am 23:937, 2005; Boudreaux ED et al: The use of performance improvement
methods to enhance emergency department patient satisfaction in the United States: a critical review of the literature
and suggestions for future research. Acad Emerg Med 13:795, 2006; Brady WJ et al: Prevalence, therapeutic response,
and outcome of ventricular tachycardia in the out-of-hospital setting: a comparison of monomorphic ventricular
tachycardia, polymorphic ventricular tachycardia, and torsades de pointes. Acad Emerg Med 6:609, 1999; Brown
AM et al: The Impact of B-Type Natriuretic Peptide in Addition to Troponin I, Creatine Kinase-MB, and Myoglobin
on the Risk Stratification of Emergency Department Chest Pain Patients With Potential Acute Coronary Syndrome.
Ann Emerg Med Nov 2, 2006; Collinson PO et al: Utility of admission cardiac troponin and "Ischemia Modified
Albumin" measurements for rapid evaluation and rule out of suspected acute myocardial infarction in the emergency
department. Emerg Med J 23:256, 2006; Hoekstra JW et al: Improving the care of patients with non-ST-elevation
acute coronary syndromes in the emergency department: the CRUSADE initiative. Acad Emerg Med 9:1146, 2002;
Katz DA et al: Emergency physicians' fear of malpractice in evaluating patients with possible acute cardiac ischemia.
Ann Emerg Med 46:525, 2005; Kontos MC et al: Imaging in the evaluation of the patient with suspected
acute coronary syndrome. Cardiol Clin 23:517, 2005; Maron MS et al: Hypertrophic Cardiomyopathy Is Predominantly
a Disease of Left Ventricular Outflow Tract Obstruction. Circulation Nov 6, 2006; Mitchell AM et al: Multimarker
panel to rule out acute coronary syndromes in low-risk patients. Acad Emerg Med 13:803, 2006; Peacock F
et al: Meta-analysis of ischemia-modified albumin to rule out acute coronary syndromes in the emergency department.
Am Heart J 152:253, 2006; Pollack CV Jr et al: Application of the TIMI risk score for unstable angina and
non-ST elevation acute coronary syndrome to an unselected emergency department chest pain population. Acad
Emerg Med 13:13, 2006; Pollack CV Jr et al: 2000 ACC/AHA guidelines for the management of patients with unstable
angina and non-ST-segment elevation myocardial infarction: a practical summary for emergency physicians.
Ann Emerg Med 38:229, 2001; Pope JH et al: The impact of electrocardiographic left ventricular hypertrophy and
bundle branch block on the triage and outcome of ED patients with a suspected acute coronary syndrome: a multicenter
study. Am J Emerg Med 22:156, 2004; Stollberger C et al: Pitfalls in the diagnosis of left ventricular hypertrabeculation/non-compaction.
Postgrad Med J 82:679, 2006; Viskin S: Torsades de Pointes. Curr Treat Options
Cardiovasc Med 1:187, 1999.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. The following
has been disclosed: Dr. Slattery is on the Speakers’ Bureaus at Genentech and Johnson & Johnson (Scios).
Dr. Slattery was recorded in Las Vegas, NV, at High Risk Emergency Medicine, held May 23-24, 2006, and sponsored
by the Center for Emergency Medical Education, the Emergency Physicians’ Medical Group, the Emergency
Medicine Physicians, and the Ohio Chapter of the American College of Emergency Physicians. Dr. Mattu was recorded
in San Francisco, at High Risk Emergency Medicine, held May 24-26, 2006, and sponsored by the University
of California, San Francisco, School of Medicine. The Audio-Digest Foundation thanks the speakers and the sponsors
for their cooperation in the production of this program.
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